Haematopathology: An introduction to the various myeloid cell neoplasms

Haematopathology
THE MYELOID NEOPLASMS
Dr Brian Mitchelson
Qatar Cardiovascular Research Centre

THE MYELOID CELL LINES
The term “myeloid” includes all cells belonging to the granulocyte (i.e.,
neutrophil, eosinophil, basophil), monocyte/macrophage, erythroid,
megakaryocyte, and mast cell lines.
Myeloid malignancies are clonal diseases of the hematopoietic stem or
progenitor cells.
These malignancies can be present in the bone marrow and peripheral
blood.
They result from genetic and epigenetic alterations that disrupt key
haematogenic processes such as self-renewal, proliferation and
impaired differentiation.
Categorization of the disorders is based on the morphology,
cytochemistry, phenotype, genetics, and clinical features of the various
myeloid disorders,

MYELOID NEOPLASMS
The World Health Organisation (WHO) categorize these as:
(1)Myelodysplastic Syndromes (MDSs)
(2) Myeloproliferative neoplasms (MPNs)
(3) Myelodysplastic/myeloproliferative neoplasms
(MDS/MPN)
(4) Myeloid malignancies associated with eosinophilia
and abnormalities of growth factor receptors derived
from platelets or fibroblasts.

Examples of Myeloid Neoplasms.
1. Acute myeloid leukemia
2. Myelodysplastic syndromes (MDS)
2.1 Refractory cytopenia with unilineage dysplasia
Refractory anemia; Refractory neutropenia;
Refractory thrombocytopenia
2.2 Refractory anemia with ring sideroblasts
2.3 Refractory cytopenia with multilineage dysplasia
2.4 Refractory anemia with excess blasts-1
2.5 Refractory anemia with excess blasts-2
2.6 Myelodysplastic syndrome with isolated deletion(5q)
2.7 Myelodysplastic syndrome, unclassifiable

3. Myeloproliferative neoplasms (MPN)
3.1 Chronic myelogenous leukemia
3.2 Polycythemia vera
3.3 Essential thrombocythemia
3.4 Primary myelofibrosis
3.5 Chronic neutrophilic leukemia
3.6 Chronic eosinophilic leukemia, not otherwise
categorized
3.7 Hypereosinophilic syndrome
3.8 Mast cell disease
3.9 MPNs, unclassifiable

4. Myelodysplastic/myeloproliferative neoplasms (MDS/MPN)
4.1 Chronic myelomonocytic leukemia
4.2 Juvenile myelomonocytic leukemia
4.3 Atypical chronic myeloid leukemia
4.4 MDS/MPN, unclassifiable
5. Myeloid neoplasms associated with eosinophilia and abnormalities
of PDGFR-A or -B, or FGFR1
5.1 Myeloid neoplasms associated with PDGFR-A or -B rearrangement
5.2 Myeloid neoplasms associated with FGFR1 rearrangement
(8p11 myeloproliferative syndrome)

1. Acute Myeloid Leukemia AML
AML is characterized by the rapid growth of abnormal
white blood cells that accumulate in the bone marrow and
interfere with the production of normal blood cells.
AML is the most common acute leukemia affecting adults,
and its incidence increases with age but is a relatively rare
disease.
The symptoms include fatigue, shortness of breath, easy
bruising and bleeding, and an increased risk of infection.
Several risk factors and chromosomal abnormalities have
been identified, but the specific cause is not clear.
As an acute leukemia, AML progresses rapidly and is
typically fatal within weeks or months if left untreated.

AML has several subtypes and the treatment and prognosis
varies among subtypes.
The five-year survival rates vary from 15–70%, and the
relapse rate varies from 33–78%, depending on subtype.
AML is treated initially with chemotherapy aimed at inducing
a remission; patients may go on to receive additional
chemotherapy or a hematopoietic stem cell transplant.
Recent research into the genetics of AML has resulted in the
availability of tests that can predict which drug or drugs may
work best for a particular patient, as well as how long that
patient is likely to survive.

Bone marrow aspirate of AML
The arrows show the presence of Auer Rods in the cytoplasm of the blast
cells. These azurophilic granular rod structures are only found in AML

A blood film from AML
Note the cell size, large off-centre nucleus and scarce cytoplasm.

A bone marrow trephine biopsy of AML
The biopsy shows presence of large numbers of the abnormal myeloblasts in the bone marrow.

Response to Lenalidomide
Therapy in AML
Bone marrow aspirate (hematoxylin and eosin – light
microscopy) at the time of diagnosis of leukemic
transformation with 34% myeloblasts.
Repeat bone marrow aspirate after 3 months of
Lenalidomide now with 5% myeloblasts, improved
granulocytic maturation and normal peripheral blood
counts.

Genetic Karyotyping of AML
The arrow shows the deletion of 7q

2. Myelodysplastic Syndromes (MDS)
MDS covers a wide range of neoplasms each with their
own characteristic features which we will see in the next
slides.

The myelodysplastic syndromes (MDS) comprise a heterogeneous
group of malignant hematopoietic stem cell disorders characterized by
dysplastic and ineffective blood cell production with a variable risk of
transformation to acute leukemia.
These disorders may occur de novo or arise years after exposure to
potentially mutagenic therapy (eg, radiation exposure, chemotherapy).
Patients with MDS have a variable reduction in the production of normal
red blood cells, platelets, and mature granulocytes. This often results in
a variety of systemic consequences including anemia, bleeding, and an
increased risk of infection.

MDS occurs most commonly in older adults with a median
age at diagnosis in most series of ≥65 years and a male
predominance.
Onset of the disease earlier than age 50 is unusual with the
exception of treatment-induced MDS but rare cases of MDS
have been reported in children at a median age of six years.
The risk of developing MDS increases with age. In one
study, the annual incidence per 100,000 was estimated to
be 0.5, 5.3, 15, 49, and 89 for individuals <50 years of age;
50 to 59; 60 to 69; 70 to 79; and >80 years, respectively
.

PATHOLOGIC FEATURES
Myelodysplastic syndrome (MDS) is characterized by abnormal cell
morphology (dysplasia) and quantitative changes in one or more of the
blood and bone marrow elements (ie, red cells, granulocytes, platelets).
CBC — Complete blood count with leukocyte differential almost always
demonstrates a macrocytic or normocytic anemia; neutropenia and
thrombocytopenia are more variable.
Pancytopenia (ie, anemia, leukopenia, and thrombocytopenia) is present at
the time of diagnosis in up to 50 percent of patients.
While isolated anemia is not uncommon, less than 5 percent of patients
present with an isolated neutropenia, thrombocytopenia, or monocytosis in
the absence of anemia.

●Anemia – Anemia is almost uniformly present and is generally associated
with an inappropriately low reticulocyte response. The mean corpuscular
volume (MCV) may be macrocytic (>100 fl) or normal. The red cell
distribution width (RDW) is often increased reflecting the presence of
increased variability in red cell size, also called anisocytosis. The mean
corpuscular haemoglobin concentration (MCHC) is usually normal,
reflecting a normal ratio of hemoglobin to cell size.
●Leukopenia – Approximately half of patients have a reduced total white
blood cell count, usually resulting from absolute neutropenia. Circulating
immature neutrophils (myelocytes, promyelocytes, and myeloblasts) may
be identified, but blasts constitute fewer than 20 percent of the differential
count.

●Thrombocytopenia – Varying degrees of thrombocytopenia are present
in roughly 25 percent of patients with MDS. Unlike anemia, isolated
thrombocytopenia is not a common early manifestation of MDS. However,
a thrombocytopenic presentation with minimal morphologic dysplasia has
been described in patients in whom del(20q) was the sole karyotypic
abnormality. Such patients may be easily misdiagnosed as having immune
thrombocytopenia (ITP).
●Thrombocytosis – Thrombocytosis is less commonly seen in MDS than
thrombocytopenia. In one report, of the 388 patients diagnosed with MDS
from 1980 to 2006 at a single institution, 31 (8 percent) presented with a
high platelet count. Among these patients, there was a low incidence of
spontaneous bleeding or thromboembolic events. Thrombocytosis has
been described in 5q- syndrome, 3q21q26 syndrome, and refractory
anaemia with ring sideroblasts and thrombocytosis (RARS-T), which is
often associated with activating mutations in JAK2.

Myelodysplastic syndromes
Refractory anemia with ring sideroblasts

Refractory cytopenia with unilineage dysplasia

Megaloblastic erythroid precursors seen on MDS display an
"open" conformation of chromatin

Bone marrow biopsy showing cells undergoing karyorrhexis
among necrotic marrow cells in a patient with advanced MDS
and progressive bone pains.

Peripheral blood smear showing leukoerythroblastic picture
with immature myeloid cells in a patient with myelodysplasia
and bone marrow necrosis.

Refractory cytopenia with multilineage dysplasia (RCMD). Bone marrow biopsy (H&E stain).
This image illustrates an abnormally small megakaryocyte with hypolobated nucleus. Note
the dense, pink-staining cytoplasm

Hypolobulated granulocytes are abundant in this marrow
from a patient with myelodysplastic syndrome.

Myelodysplastic syndrome
Megakaryocyte with multiple abnormal lobes. Some of these
are disconnected.

Myelodysplastic syndrome
Refractory cytopenia with multilineage dysplasia

3. Myeloproliferative Neoplasms
(MPN)
The myeloproliferative neoplasms (MPNs), are
characterized by the clonal proliferation of
one or more hematopoietic cell lineages,
predominantly in the bone marrow, but
sometimes in the liver and spleen.
In contrast to myelodysplastic syndromes
(MDS), MPNs demonstrate terminal myeloid
cell expansion into the peripheral blood.

There are six different types of MPN. They are generally distinguished from each
other by the type of cell which is most affected. These are:
1.Polycythemia vera - an overproduction of red blood cells
2.Essential thrombocythemia - overproduction of platelets
3. Chronic myelomonocytic leukaemia (CMML) - overproduction of white
cells granulocytes)
4.Chronic neutrophilic leukaemia - overproduction of neutrophils
5.Chronic eosinophilic leukaemia - overproduction of eosinophils.
6. Idiopathic myelofibrosis - a condition in which bone marrow tissue is
gradually replaced by fibrous scar-like tissue, disrupting normal blood cell
production

In many cases these diseases develop slowly and get
worse gradually. In some cases myeloproliferative
neoplasms can progress to leukaemia.
Treatment depends on the type of MPN, the severity,
general health and age of the person diagnosed.
Treatment is generally aimed at reducing the excessive
number of blood cells in circulation, and at preventing and
treating the symptoms and complications of the disease.

Polycythaemia Vera
Polycythaemia (Rubra) Vera, also known as primary polycythaemia vera,
is a disorder where too many red cells are produced in the bone marrow,
without any identifiable cause.
These cells accumulate in the bone marrow and in the blood stream
where they increase the blood volume and cause the blood to become
thicker, or more 'viscous' than normal.
In many people with polycythaemia vera, too many platelets and white
cells are also produced.
Polycythaemia vera is a rare chronic disease diagnosed in an estimated 2
to 3 people per 100,000 population. Although it can occur at any age,
polycythaemia vera usually affects older people, with most patients
diagnosed over the age of 55 years. Polycythaemia vera is rare in children
and young adults. It occurs more commonly in males than in females.

Diagnosis
Polycythaemia vera is diagnosed using a combination of laboratory tests and a
physical examination.
Full blood count
People with polycythaemia vera have a high red cell count, haemoglobin level and
haematocrit (>52 % in men or >48% in females) due to the excessive production of
red cells. The haematocrit is the percentage of the whole blood that is made up of red
cells. A raised white cell count (especially a raised neutrophil count) and a raised
platelet count are also common findings.
The Red Cell Mass is the total number of red cells circulating in your blood.
Polycythaemia vera may be diagnosed when the red cell mass is 25% greater than
the average normal expected value. Other findings that help confirm the diagnosis of
polycythaemia vera include an enlarged spleen (splenomegaly) and the presence of
the JAK2 mutation or other cytogenetic abnormalities in your blood or bone marrow
cells.

JAK2 Mutation testing
JAK2 mutations (particularly the V617F mutation) can be found in more
than 95% of people with Polycythaemia vera. This test can be performed
on a blood sample and will help to confirm the diagnosis of a
myeloproliferative neoplasm. It doesn't help distinguish polycythaemia
vera from essential thrombocythaemia or primary myelofibrosis.
Bone marrow examination
In polycythaemia vera the bone marrow is often very active with
abnormally high numbers of normal cells. Iron stores may be depleted
since iron is being used to make more and more red cells

Bone Marrow biopsy –Polycythemia Vera
The bone marrow in polycythemia vera is hypercellular as a result
of an increase in myeloid, erythroid, and megakaryocytic elements.

Essential Thrombocythemia (ET)
ET is characterized by a sustained clonal proliferation of megakaryocytes in
the bone marrow8, with a peripheral blood platelet count greater than 600 x
109/L.
This platelet count threshold has been decreased to greater than 450 x
109/L in the most recent WHO classification.
Causes of reactive thrombocytosis must be excluded. The underlying cause
of the disease is unknown.
Epidemiology
The incidence of the disease is approx. 2.5/100,000 population per year and
is the lowest among the chronic MPNs.
There may be a higher prevalence in younger women.
The median age at diagnosis is 60 years.

Pathophysiology
The proliferation of megakaryocytes is primarily caused by clonal stem
cells, as confirmed by enzyme and genetic analysis.
Megakaryocyte progenitor cells in ET are hypersensitive to the action of
several cytokines, including IL-3 and IL-6, and possibly thrombopoietin.
This leads to increased platelet production. There is controversy
regarding spontaneous megakaryocyte formation in ET.
The JAK2 mutation is found in 50% to 60% of ET patients.
Patients lacking mutations in JAK2 may instead demonstrate activating
mutations of the thrombopoietin receptor, MPL, MPL W515K or MPL
W515L.2

Diagnosis
Patients need to fulfill the following criteria:
(1)Platelet count >600 x 109/L;
(2)Megakaryocytic hyperplasia on bone marrow aspiration and
biopsy,
(3)Absence of the Philadelphia chromosome;
(4)Absence of infection, inflammation, and other causes for
reactive thrombocytosis;
(5)Normal red blood cell mass or a haemoglobin concentration
<13 g/dL;
(6)The presence of stainable iron in a bone marrow aspiration
or ≤1 g/dL increase in haemoglobin concentration after a one
month trial of oral iron therapy.

ET Blood Film
Although some variation in platelet size is present, the platelets are not
otherwise atypical but show a significant increase in numbers.

ET Bone Marrow Trephine Biopsy
Megakaryocytes in essential thrombocythemia are not only
increased in size and number but also have deeply lobulated
and hyperlobated nuclei and tend to form small clusters.

Chronic Myelomonocytic
Leukaemia (CMML)
Pathophysiology
CMML is a clonal disorder of a bone marrow stem cell line.
Monocytosis is a major defining feature.
CMML exhibits heterogenous clinical, haematological, and morphologic
features, varying from predominantly myelodysplastic to predominantly
myeloproliferative.

Diagnosis
CMML is characterized pathologically by the following:
1.Persistent monocytosis is greater than 1×109/L in the
peripheral blood.
2.No Philadelphia chromosome or BCR/ABL fusion gene.
3.Fewer than 20% blasts in the blood or bone marrow.
4. Dysplasia involving one or more myeloid lineages or, if
myelodysplasia is absent or minimal, either an acquired clonal
cytogenetic bone marrow abnormality or at least 3 months of
persistent peripheral blood monocytosis, if all other causes
are ruled out.

Bone Marrow Trephine Biopsy CMML
Monocytic elements are increased in this bone marrow
aspirate

Blood Film from CMML
Monocytosis and the presence of myelocytes, metamyelocytes and
promyelocytes is typical of CMML

Chronic Neutrophilic Leukaemia
(CNL)
Chronic neutrophilic leukemia (CNL) is a rare chronic
myeloproliferative neoplasm of unknown etiology
It is characterized by sustained peripheral blood
neutrophilia (>25 × 109/L) and hepatosplenomegaly.
The bone marrow is hypercellular.
No significant dysplasia is found in any of the cell
lineages, and bone marrow fibrosis is uncommon.

Diagnosis
Cytogenetic studies are normal in nearly 90% of the patients.
In the remaining patients, clonal karyotypic abnormalities may
include +8, +9, del (20q) and del (11q).
There is no Philadelphia chromosome or BCR/ABL fusion
gene.
CNL is a slowly progressive disorder, and the survival of
patients is variable, ranging from 6 months to more than 20
years.

Bone marrow smear from CNL
Bone marrow smears show increased granulocytic elements
with predominance of segmented neutrophils and bands

Peripheral Blood Film CNL
Chronic neutrophilic leukemia. The peripheral blood smear shows an absolute neutrophilia
without the significant left shift, vacuolization, or toxic granulation usually associated with
a reactive process. Döhle bodies (arrows) are often present in the cytoplasm of neutrophils

Chronic Eosinophilic Leukaemia
(CEL)
Chronic eosinophilic leukemia is a disease in which too
many white blood cells (eosinophils) are produced in the
bone marrow.
In chronic eosinophilic leukemia, there are too many
eosinophils in the blood, bone marrow, and other tissues.
There is no dysplasia of the eosinophils.
Chronic eosinophilic leukemia may stay the same for
many years or it may progress quickly to acute leukemia.

Diagnosis
The main criteria for diagnosing eosinophilic leukemia are:
An eosinophil count in the blood of 1.5 x 109 /L or higher that lasts over
time.
No parasitic infection, allergic reaction, or other causes of eosinophilia.
In addition to a physical examination, the following tests may be used to
diagnose eosinophilic leukemia:
Blood tests.
The diagnosis of eosinophilic leukemia begins with a complete blood
count (CBC).
If the blood contains many eosinophils (see criteria above), eosinophilic
leukemia is suspected.

Bone marrow aspiration and biopsy.
Many immature cells, blast cells, in the bone marrow are a sign of acute rather
than chronic eosinophilic leukemia.
Molecular testing
If an eosinophilia is found, a molecular genetic analysis should be done to test
for the mutation FIP1-like platelet-derived growth factor alpha.
Cytogenetics may also be used to determine any abnormality and also to guide
a suitable treatment regime.

Chronic Eosinophilic Leukemia
Bone marrow biopsy showing eosinophilia

Chronic Eosinophilic Leukemia
Peripheral blood film – a significant increase in the number
of eosinophils in circulation.

Idiopathic Myelofibrosis MF
Myelofibrosis is a rare condition that affects the bone
marrow.
In MF, scar tissue builds up inside the bone marrow and
blood cells are not produced properly or in the correct
numbers.
It can affect people at any age, including children, but it's
most common in people over 50.

MF can occur in people who haven’t any history of problems with their bone
marrow. This is called primary myelofibrosis. MF can also develop in people who
have essential thrombocythaemia (ET) or polycythaemia vera (PV). This is called
post-ET myelofibrosis or post-PV myelofibrosis.
These are all called myelofibrosis as they behave in the same way.
People with MF may have low levels of one or more types of blood cells. If the
bone marrow becomes scarred (fibrosed), it may make fewer blood cells. Some
people have too few of some types of blood cells and too many of another type.
To make up for fewer blood cells being made in the bone marrow, other parts of
the body, usually the spleen and liver, begin to make blood cells. As the spleen
begins to make blood cells, it grows in size.
The enlarged spleen may ‘hold on’ to blood cells, instead of releasing them into
the blood. The spleen may also destroy blood cells. This can reduce the numbers
of blood cells in the blood.

Diagnosis
Tests and investigations that may be done to confirm a diagnosis of MF include:
JAK2 test
This blood test checks for a change (mutation) in a gene called JAK2 which helps
control how many blood cells are made. A spontaneous mutation in the gene, which
happens during the person's lifetime, can cause MF. This is a non-hereditary
mutation
CALR blood test
Blood tests might also check for a change in another gene called calreticulin (CALR).
As with the JAK2 gene change, it happens during the person's lifetime. Again this is
non-hereditary.
Bone marrow sample (biopsy and smear)

Idiopathic Myelofibrosis
A bone marrow trephine biopsy showing the increased fibrous
tissue (stained black) within the bone marrow spaces

Idiopathic Myelofibrosis
Bone marrow biopsy showing extensive fibrosis with few
germinal cells.

Juvenile Myelomonocytic
Leukaemia JMML
Juvenile myelomonocytic leukemia (JMML) is a rare
childhood cancer that usually occurs in children younger
than 2 years old.
In JMML, too many myelocytes and monocytes (two types
of WBCs) are produced from immature blast stem cells.
These myelocytes, monocytes, and blasts overwhelm the
normal red and white cell production in the bone marrow
and other organs, causing the symptoms of JMML.

Diagnosis
Blood tests.
Tests such as a complete blood count, liver and kidney
function panels, and blood chemistries can give important
information about the number of normal blood cells in the
body and how well the organs are functioning.
The blood film will also be examined under a microscope to
check for abnormal shapes or sizes.
Bone marrow aspiration.
This will also be examined microscopically for abnormal
cells.

Juvenile myelomonocytic leukemia
Note the large numbers of both immature myeloid
neutrophils and monocytes.

Juvenile myelomonocytic leukemia
Note the bizarre nuclear lobulation of the cell types

Atypical Chronic Myeloid
Leukaemia (aCML)
aCML is a chronic myeloproliferative disorder with a clinical
and hematological picture similar to chronic myelogenous
leukemia (CML) but lacking Philadelphia chromosome
and BCR - ABL or PDGFR-B rearrangements.
Atypical CML is characterized by the combination of: 10-
20% of immature granulocytes; marked granulocytic
dysplasia and both less than 2% of basophils and less than
10% of monocytes.

Diagnosis
Peripheral blood film:
This shows a leukocytosis with a high count of immature
granulocytes.
By definition monocytes are less than 10% and
basophils less than 2%.
Anemia is more frequent than thrombocytopenia.
Bone marrow:
Hypercellular with myelodysplastic features of the three
series, most marked in granulocytic lineage. Blast cell
infiltration ranges from 0% to 10%.

Atypical Chronic Myeloid Leukaemia
Marked granulocytic hyperplasia and dysplasia (convoluted
lobulation of nuclei, pseudo-Pelger-Huet forms), <20% blasts

Abnormal chromatin clumping. Note neutrophils with abnormal condensation
of the nuclear chromatin, which is the hallmark of this condition.

MDS/MPN, unclassifiable
Myelodysplastic/Myeloproliferative Unclassifiable Neoplasm:
(MDS/ MPN-UC)
This is also known as mixed myeloproliferative/ myelodysplastic
syndrome, which does not fit a single criterion but is
unclassifiable with overlapping feature of both syndromes.
It shows features of both myeloproliferative disease and
myelodysplastic disease but does not meet the criteria for any
of the other MDS/MPN entities.

Diagnosis
Diagnostic criteria for MDS/MPN-UC can be either:
The combination of four sets of criteria (a–d):
A.Clinical, laboratory, and morphologic features of
myelodysplastic syndrome (MDS) (e.g., refractory anemia,
refractory anemia with ringed sideroblasts, refractory
cytopenia with multilineage dysplasia, and refractory
anemia with excess of blasts) with fewer than 20% blasts
in the blood and bone marrow.
B.Prominent myeloproliferative features, e.g. platelet count
greater than 600 × 109/L associated with megakaryocytic
proliferation, or white blood cell count greater than 13.0 × 109/L
with or without splenomegaly.

C. No history of an underlying chronic myeloproliferative
disorder (CMPD), MDS, or recent cytotoxic or growth factor
therapy that could cause the myelodysplastic or
myeloproliferative features.
D. No Philadelphia chromosome or BCR/ABL fusion gene,
del(5q), t(3;3)(q21;q26), or inv(3)(q21q26).
or:
Mixed myeloproliferative and myelodysplastic features that
cannot be assigned to any other category of MDS, CMPD, or
MDS/MPN.

Bone Marrow biopsy reveals a hypercellularity (100%) with markedly increased
myeloid: erythroid ratio (26:1). Dysplastic megakaryocytes are indicated by arrows.

marked leukocytosis with many myeloid precursors
:promyelocytes, myelocytes, and metamyelocytes,

Myeloid neoplasms associated with PDGFR-A or -B
rearrangement and myeloid neoplasms associated
with FGFR1 rearrangement (8p11 myeloproliferative
syndrome)
There are three main myeloproliferative and
lymphoid neoplasms associated with the
rearrangement of the PDGFR-A, PDGFR-B and
FGFR-1 genes.

All result from the formation of a fusion gene encoding an
aberrant tyrosine kinase.
This disease is associated with PDGFRA rearrangement
that is associated with FIP1L1-PDGFRA formed as a
result of a cryptic deletion at 4q12.
Presentation is generally as chronic eosinophilic leukemia
(CEL) but can be acute myeloid leukemia (AML) as well.

Diagnosis
Definitive Diagnostic Methods:
Bone marrow
FISH ( Fluorescent in-situ hybridisation)
Genetic testing
Immunophenotyping

Myeloid neoplasms associated with PDGFR-A or -B rearrangement and
myeloid neoplasms associated with FGFR1 rearrangement
The peripheral blood film showed many morphologic abnormalities of
eosinophils, including of size, granulation, and nuclear lobulation.

Myeloid neoplasms associated with PDGFR-A or -B rearrangement
and myeloid neoplasms associated with FGFR1 rearrangement
The arrow shows a blast cell in the peripheral blood.

The End of Part 2
Thank you
I would like to thank the following for the use of several images and data:
Lichtman’s Atlas of Hematology
The American Society of Hematology
Weill Cornel University
Hematopathology for medical education – WebPath
Atlas of Hematopathology | 978-0-12-385183-3 | Elsevier

Haematopathology: An introduction to the various myeloid cell neoplasms

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Viewers also liked

Viewers also liked (20)

Similar to Haematopathology: An introduction to the various myeloid cell neoplasms

Similar to Haematopathology: An introduction to the various myeloid cell neoplasms (20)

More from Qatar Cardiovascular Research Centre

More from Qatar Cardiovascular Research Centre (7)

Recently uploaded

Recently uploaded (20)

Haematopathology: An introduction to the various myeloid cell neoplasms

Editor's Notes